• cardiology
• medical research

• Animals
• Asphyxia/complications
• Capnography
• Carbon Dioxide
• Cardiopulmonary Resuscitation
• Disease Models, Animal
• Heart Arrest/therapy
• Heart Arrest/complications
• Out-of-Hospital Cardiac Arrest/complications
• Return of Spontaneous Circulation
• Swine

• Instituto de Salud Carlos III

Mean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest.

Twenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5–7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min.

After the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO₂, each mmHg increase in PaCO_2, and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg (p < 0.001) and decreased by 0.031 mmHg and 0.013 mmHg (p < 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5–7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905, p < 0.001).

Mean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5–7.5 s after cardiac arrest can highly predict ROSC.

The online version contains supplementary material available at 10.1186/s40635-022-00440-z.

• Drowning
• Hypoxia
• Mouth-to-Mouth
• Pulmonary shunt
• Resuscitation

• cardiopulmonary resuscitation
• resuscitation
• ventilation

• Attitude of Health Personnel
• Cardiopulmonary Resuscitation/methods
• Child, Preschool
• China
• Clinical Competence
• Female
• Health Care Surveys
• Heart Arrest/therapy
• Humans
• Infant
• Intensive Care Units, Pediatric
• Internationality
• Male
• Oxygen/administration & dosage
• Oxygen Consumption/physiology
• Patient Care Team
• Pulmonary Ventilation/physiology
• Respiration, Artificial/methods
• Risk Factors
• Surveys and Questionnaires
• Treatment Outcome

Chest compressions (CC) during cardiopulmonary resuscitation are not sufficiently effective in many circumstances. Mechanical CC could be more effective than manual CC, but there are no studies comparing both techniques in children. The objective of this study was to compare the effectiveness of manual and mechanical chest compressions with Thumper device in a pediatric cardiac arrest animal model.

An experimental model of asphyxial cardiac arrest (CA) in 50 piglets (mean weight 9.6 kg) was used. Animals were randomized to receive either manual CC or mechanical CC using a pediatric piston chest compressions device (Life-Stat®, Michigan Instruments). Mean arterial pressure (MAP), arterial blood gases and end-tidal CO2 (etCO2) values were measured at 3, 9, 18 and 24 minutes after the beginning of resuscitation.

There were no significant differences in MAP, DAP, arterial blood gases and etCO2 between chest compression techniques during CPR. Survival rate was higher in the manual CC (15 of 30 = 50%) than in the mechanical CC group (3 of 20 = 15%) p = 0.016. In the mechanical CC group there was a non significant higher incidence of haemorrhage through the endotracheal tube (45% vs 20%, p = 0.114).

In a pediatric animal model of cardiac arrest, mechanical piston chest compressions produced lower survival rates than manual chest compressions, without any differences in hemodynamic and respiratory parameters.

• Animals
• Asphyxia/complications
• Cardiopulmonary Resuscitation/methods
• Heart Arrest/etiology
• Heart Arrest/therapy
• Swine

• Instituto de Salud Carlos III

Actual resuscitation guidelines recommend 10 respirations per minute (rpm) for advanced pediatric life support. This respiratory rate (RR) is much lower than what is physiological for children. The aim of this study is to compare changes in ventilation, oxygenation, haemodynamics and return of spontaneous circulation (ROSC) rates with three RR.

An experimental model of asphyxial cardiac arrest (CA) in 46 piglets (around 9.5 kg) was performed. Resuscitation with three different RR (10, 20 and 30 rpm) was carried out. Haemodynamics and gasometrical data were obtained at 3, 9, 18 and 24 minutes after beginning of resuscitation. Measurements were compared between the three groups.

No statistical differences were found in ROSC rate between the three RR (37.5%, 46.6% and 60% in the 10, 20 and 30 rpm group respectively P = 0.51). 20 and 30 rpm groups had lower PaCO2 values than 10 rpm group at 3 minutes (58 and 55 mmHg vs 75 mmHg P = 0.08). 30 rpm group had higher PaO2 (61 mmHg) at 3 minutes than 20 and 10 rpm groups (53 and 45 mmHg P = 0.05). No significant differences were found in haemodynamics or tissue perfusion between hyperventilated (PaCO2 <30 mmHg), normoventilated (30–50 mmHg) and hypoventilated (>50 mmHg) animals. PaO₂ was significantly higher in hyperventilated (PaO₂ 153 mmHg) than in normoventilated (79 mmHg) and hypoventilated (47 mmHg) piglets (P<0.001).

Our study confirms the hypothesis that higher RR achieves better oxygenation and ventilation without affecting haemodynamics. A higher RR is associated but not significantly with better ROSC rates.

• Age Factors
• Animals
• Cardiopulmonary Resuscitation
• Disease Models, Animal
• Heart Arrest/physiopathology
• Respiratory Rate
• Swine

• Instituto de Salud Carlos III
• Promotion and the European Regional Development Fund (ERDF)

The pressure-recording analytical method is a new semi-invasive method for cardiac output measurement (PRAM). There are no studies comparing this technique with femoral artery thermodilution (FATD) in an infant animal model.

A prospective study was performed using 25 immature Maryland pigs weighing 9.5 kg. Fifty-eight simultaneous measurements of cardiac index (CI) were made by FATD and PRAM at baseline and after return of spontaneous circulation. Differences, correlation, and concordance between both methods were analyzed. The ability of PRAM to track changes in CI was explored with a polar plot.

Mean CI measurements were 4.5 L/min/m² (95 % CI, 4.2–4.8 L/min/m²; coefficient of variation, 27 %) by FATD and 4.0 L/min/m² (95 % CI, 3.6–4.3 L/min/m²; coefficient for variation, 37 %) by PRAM (difference, 0.5 L/min/m²; 95 % CI for the difference, 0.1–1.0 L/min/m²; p = 0.003; n = 58). No correlation between both methods was observed (r = 0.170, p = 0.20). Limits of agreement were −2.9 to 4.0 L/min/m² (−69.9 to 84.9 %). Percentage error was 80.6 %. Only 26.1 % of data points lied within an absolute deviation of ±30° from the polar axis.

No correlation nor concordance between both methods was observed. Limits of agreement and percentage of error were high and clinically not acceptable. No concurrence between both methods in CI changes was observed. PRAM is not a useful method for measurement of the CI in this pediatric model of cardiac arrest.

• Cardiac arrest
• Cardiac index
• Cardiac output
• Children
• Infant animal model
• Pressure recording analytical method

• Algorithms
• Animals
• Duodenum
• Esophagus
• Female
• Heart Rate/physiology
• Humans
• Monitoring, Ambulatory/instrumentation
• Monitoring, Ambulatory/methods
• Respiratory Rate/physiology
• Stomach
• Swine
• Telemedicine/instrumentation
• Wireless Technology/instrumentation

• R01 EB000244 NIBIB NIH HHS
• T32 DK007191 NIDDK NIH HHS
• 27306C0002 NIEHS NIH HHS
• 27304C0002 NIEHS NIH HHS
• T32DK7191-38-S1 NIDDK NIH HHS
• R37 EB000244 NIBIB NIH HHS
• EB000244 NIBIB NIH HHS

• Arrhythmias, Cardiac/complications
• Arrhythmias, Cardiac/physiopathology
• Arrhythmias, Cardiac/therapy
• Asphyxia/complications
• Asphyxia/physiopathology
• Asphyxia/therapy
• Heart Arrest/diagnosis
• Heart Arrest/etiology
• Heart Arrest/therapy
• Humans
• Resuscitation

Cardiac arrest remains a leading cause of death and permanent disability worldwide. Although many victims are initially resuscitated, they often succumb to the extensive ischemia-reperfusion injury inflicted on the internal organs, especially the brain. Cardiac arrest initiates a complex cellular injury cascade encompassing reactive oxygen and nitrogen species, Ca²⁺ overload, ATP depletion, pro- and anti-apoptotic proteins, mitochondrial dysfunction, and neuronal glutamate excitotoxity, which injures and kills cells, compromises function of internal organs and ignites a destructive systemic inflammatory response. The sheer complexity and scope of this cascade challenges the development of experimental models of and effective treatments for cardiac arrest. Many experimental animal preparations have been developed to decipher the mechanisms of damage to vital internal organs following cardiac arrest and cardiopulmonary resuscitation (CPR), and to develop treatments to interrupt the lethal injury cascades. Porcine models of cardiac arrest and resuscitation offer several important advantages over other species, and outcomes in this large animal are readily translated to the clinical setting. This review summarizes porcine cardiac arrest-CPR models reported in the literature, describes clinically relevant phenomena observed during cardiac arrest and resuscitation in pigs, and discusses numerous methodological considerations in modeling cardiac arrest/CPR. Collectively, published reports show the domestic pig to be a suitable large animal model of cardiac arrest which is responsive to CPR, defibrillatory countershocks and medications, and yields extensive information to foster advances in clinical treatment of cardiac arrest.

• Acidemia
• Asphyxia
• Cardiopulmonary resuscitation
• Countershocks
• Hyperoxia
• Vasopressin
• Ventricular fibrillation

• R01 NS076975 NINDS NIH HHS
• T32 AG020494 NIA NIH HHS

• asphyxia
• cardiac arrest
• cardiopulmonary resuscitation
• catecholamines
• epinephrine
• norepinephrine